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首页> 外文期刊>Cell cycle >Autophagy is activated, but is not required for the G0 function of BCL-2 or BCL-xL.
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Autophagy is activated, but is not required for the G0 function of BCL-2 or BCL-xL.

机译:自噬已激活,但对于BCL-2或BCL-xL的G0功能不是必需的。

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摘要

Cell cycle arrest in G(0) and autophagy have features in common, but the inter-relationship between the two processes is not well defined. The anti-apoptosis molecules BCL-2 and BCL-x(L) promote G(0) arrest through upregulation of p27 protein, which can also induce autophagy. We tested the hypothesis that autophagy was involved in the cell cycle arrest function of BCL-2 and BCL-x(L). We found that in IL-3-dependent FL5.12 cells, NIH3T3 cells and mouse embryo fibroblasts induced to arrest, treatment with 3-methyladenine did not affect the expected decrease in cell size and ribosomal RNA synthesis, or upregulation of p27 levels. Using the m5-7 ATG5(-/-) MEF cell line with doxycycline-regulated ATG5 expression, we demonstrated that autophagy was activated during serum withdrawal and contact inhibition, but inhibition of autophagy had no measurable effect on G(0) arrest in parental or BCL-x(L)-expressing cells. Thus, our data indicate that, in cell culture models, autophagy occurs but is not required for entrance into quiescence or for the G(0) function of BCL-2 or BCL-x(L).
机译:G(0)中的细胞周期停滞和自噬具有共同的特征,但是两个过程之间的相互关系尚不明确。抗凋亡分子BCL-2和BCL-x(L)通过上调p27蛋白来促进G(0)阻滞,这也可以诱导自噬。我们测试了自噬参与BCL-2和BCL-x(L)的细胞周期阻滞功能的假说。我们发现,在依赖IL-3的FL5.12细胞,NIH3T3细胞和小鼠胚胎成纤维细胞被诱导逮捕后,用3-甲基腺嘌呤处理不会影响预期的细胞大小减少和核糖体RNA合成或p27水平上调。使用具有强力霉素调节的ATG5表达的m5-7 ATG5(-/-)MEF细胞系,我们证明自噬在血清停药和接触抑制过程中被激活,但是自噬的抑制对父母中G(0)阻滞没有可测量的作用或BCL-x(L)表达细胞。因此,我们的数据表明,在细胞培养模型中,发生自噬,但是进入静止状态或BCL-2或BCL-x(L)的G(0)功能不是必需的。

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